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SIX6 knockdown in Jurkat-Cas9 T-ALL cell line

ABSTRACT: SIX6 knockdown in Jurkat-Cas9 T-ALL cell line

PROVIDER: PRJNA625294 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11544652_1.fastq.gz	Fastqsanger.gz
	SRR11544652_2.fastq.gz	Fastqsanger.gz
	SRR11544653_1.fastq.gz	Fastqsanger.gz
	SRR11544653_2.fastq.gz	Fastqsanger.gz
	SRR11544654_1.fastq.gz	Fastqsanger.gz

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SIX6 knockdown in Jurkat-Cas9 T-ALL cell line

Project description:T cell acute lymphoblastic leukemia (T-ALL) is a hematological malignancy strongly affected by the abnormal activity of transcription factors. Here we report a high expression of developmental transcription factor SIX6 in TAL1 subtype of T-ALL. Our data indicates that this high expression is directly regulated by binding of TAL1 and GATA3 transcription factors into an upstream enhancer element. We also looked into the potential targets of SIX6 in T-ALL and Crispr-cas9 mediated knockout of SIX6 in Jurkat cells caused significant changes in the expression of multiple genes, including genes related to mTOR signaling. In two independent patient cohorts, the high SIX6 expression shows a trend of less favourable prognosis. However, the knockout of SIX6 was not enough to have an effect on proliferation, cell cycle or viability of the Jurkat cells and overexpression of SIX6 in the T-ALL zebrafish model didn’t influence the progression of the disease. Our results show that high expression of SIX6 has a trend towards a less favourable outcome, but SIX6 doesn’t have an independent oncogenic role in T-ALL.

2020-04-15 | GSE148658 | GEO

PRMT7 knockdown in Jurkat-Cas9 and Molt-4 T-ALL cell line

Project description:PRMT7 knockdown in Jurkat-Cas9 and Molt-4 T-ALL cell line

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Transcriptome analysis of Jurkat T-ALL clones from control and CBAP-knockdown/knockout sets

Project description:We sequenced whole-genome mRNA from 8 different single stable clones of Jurkat cells modified with CBAP gene expression usng shRNA knockdown or CRISPR/Cas9-mediated knockout and their controls.

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Gene expression profile of human T-ALL cell line JURKAT after TRIB2 knockdown

Project description:To dissect molecular pathways regulated by TRIB2 in T-ALL, we performed microarray gene expression profiling in the TAL1-positive T-ALL cells (Jurkat) after TRIB2 knockdown.

2015-08-14 | GSE66013 | GEO

Identification of LEDGF-responsive genes in Jurkat cells

Project description:The LEDGF transcript from the PSIP1 gene was knocked down in Jurkat cells using RNAi technology. The resulting Jurkat-derived cell line (Jurkat-siJK2) was compared to a control cell line (wild type Jurkat) using microarray analysis. Genes identified as being modulated by LEDGF were preferential targets of HIV integration. Keywords: effects of gene knockdown

2007-04-13 | GSE7508 | GEO

RNA-seq analysis in ARIEL knockdown Jurkat samples

Project description:RNA-seq analysis in ARIEL knockdown Jurkat samples

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The Transcriptome of over expressed SLAMF6 isoform-3 in activated Jurkat cell line

Project description:SLAMF6 is a homotypic receptor of the Ig-superfamily associated with progenitor exhausted T cells. In humans, SLAMF6 has three splice isoforms involving its V-domain.We KO isoform 1 of SLAMF6 in a Jurkat cell line and harvest this cell line RNA using Bulk-RNA-Seq after activation in 5 time points. Comparing the results to WT Jurkat cell line, we analyzed the transcriptional landscape and showed that after activation SLAMF6 isoform 3 is the prominent expressed isoform, and that the KO Jurkat cells have a stronger cytotoxic phenotype.

2020-11-05 | GSE160817 | GEO

CRISPR/Cas9 knock down line

Project description:CRISPR/Cas9 knock down line

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Transcription profiling by array of human Jurkat T cells either over-expressing miR-146a or with miR-146a knockdown

Project description:Screening the differetial expressed genes with Jurkat-146a(miR-146a over expression),Jurkat-sponge(miR-146a knockdown),Jurkat-FF3(vector control)

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PRMT7 knockdown in Jurkat-Cas9 and Molt-4 T-ALL cell line

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with only few established prognostic biomarkers.In this study, we examined the expression of protein arginine methyltransferases across hematological malignancies and discovered high levels of PRMT7 mRNA in T-ALL, particularly in the mature subtypes of T-ALL. High PRMT7 was associated with decreased event-free and overall survival in two independent patient cohorts. Genetic deletion of PRMT7 by CRISPR-Cas9 significantly decreased the colony-forming capacity of the cells and negatively impacted cell viability. In the knockout cells, alterations were seen in the monomethyl arginine levels in proteins associated with RNA processing. These results suggest that PRMT7 plays an active role in T-ALL pathogenesis.

2021-10-22 | GSE186238 | GEO

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